Journal
RICE
Volume 6, Issue -, Pages -Publisher
SPRINGER
DOI: 10.1186/1939-8433-6-1
Keywords
Rice; Lesion mimic mutant; spl5; Proteomics; 2-DE
Categories
Funding
- National Key Programs for Transgenic Crops [2011ZX08009-003]
- National Natural Science Foundation of China [31171519, 31101130]
- Natural Science Foundation of Zhejiang Province [Y3110234, Y3110230]
- Welfare Technology Application Research Project of Zhejiang Province [2011C22005]
- Zhejiang Province Key Innovative Research Team Program [2010R50024]
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Background: A lesion-mimic mutant in rice (Oryza sativa L.), spotted leaf 5 (spl5), displays a disease-resistance-enhanced phenotype, indicating that SPL5 negatively regulates cell death and resistance responses. To understand the molecular mechanisms of SPL5 mutation-induced cell death and resistance responses, a proteomics-based approach was used to identify differentially accumulated proteins between the spl5 mutant and wild type (WT). Results: Proteomic data from two-dimensional gel electrophoresis showed that 14 candidate proteins were significantly up-or down-regulated in the spl5 mutant compared with WT. These proteins are involved in diverse biological processes including pre-mRNA splicing, amino acid metabolism, photosynthesis, glycolysis, reactive oxygen species (ROS) metabolism, and defense responses. Two candidate proteins with a significant up-regulation in spl5 - APX7, a key ROS metabolism enzyme and Chia2a, a pathogenesis-related protein - were further analyzed by qPCR and enzyme activity assays. Consistent with the proteomic results, both transcript levels and enzyme activities of APX7 and Chia2a were significantly induced during the course of lesion formation in spl5 leaves. Conclusions: Many functional proteins involving various metabolisms were likely to be responsible for the lesion formation of spl5 mutant. Generally, in spl5, the up-regulated proteins involve in defense response or PCD, and the down-regulated ones involve in amino acid metabolism and photosynthesis. These results may help to gain new insight into the molecular mechanism underlying spl5-induced cell death and disease resistance in plants.
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